Bottom Line:
The ability of ESBL strains to evoke ROS-production from PMN cells was significantly higher than that of the non-ESBL strains.The number of migrating PMN was significantly higher in response to ESBL strains compared to non-ESBL strains.Stimulation of A498 cells with ESBL strains elicited lower production of IL-6 and IL-8 compared to non-ESBL strains.

Background: Infections caused by extended spectrum beta-lactamases (ESBL)-producing bacteria have been emerging worldwide and the majority of ESBL-producing E. coli strains are isolated from patients with urinary tracts infections. The purpose of this study was to compare the host-response mechanisms in human polymorphonucleated leukocytes (PMN) and renal epithelial cells when stimulated by ESBL- or non-ESBL-producing uropathogenic E. coli (UPEC) isolates. The host-pathogen interaction of these ESBL-producing strains in the urinary tract is not well studied.

Results: The ability of ESBL strains to evoke ROS-production from PMN cells was significantly higher than that of the non-ESBL strains. The growth of ESBL strains was slightly suppressed in the presence of PMN compared to non-ESBL strains after 30 min and 2h, but the opposite was observed after 5 and 6h. The number of migrating PMN was significantly higher in response to ESBL strains compared to non-ESBL strains. Stimulation of A498 cells with ESBL strains elicited lower production of IL-6 and IL-8 compared to non-ESBL strains.

Conclusion: Significant differences in host-response mechanisms were identified when host cells were stimulated by ESBL- or non-ESBL producing strains. The obtained results on the early interactions of ESBL-producing strains with the host immune system may provide valuable information for management of these infections.

Mentions:
A transepithelial migration assay was performed in order to examine PMN migration evoked by the different E. coli strains. The transwell cell monolayer showed low levels of PMN migration in the absence of bacteria (data not shown). All strains evoked PMN migration after 1 h but there were differences in their ability to attract the PMN (Figure 3A). The ESBL-induced PMN migration was significantly higher 1.6 ± 0.13 fold (p < 0.001) than the migration induced by susceptible strains (Figure 3B). The MG1655 strain induced a significant higher 3.3 ± 0.44 fold (p < 0.001) migration than the CFT073 strain. MG1655 was also shown to attract the largest number of PMN compared to the other strains (Figure 3B). There were no differences observed between ESBL-producing and susceptible strains in their ability to attract PMN after 3 h (data not shown).

Mentions:
A transepithelial migration assay was performed in order to examine PMN migration evoked by the different E. coli strains. The transwell cell monolayer showed low levels of PMN migration in the absence of bacteria (data not shown). All strains evoked PMN migration after 1 h but there were differences in their ability to attract the PMN (Figure 3A). The ESBL-induced PMN migration was significantly higher 1.6 ± 0.13 fold (p < 0.001) than the migration induced by susceptible strains (Figure 3B). The MG1655 strain induced a significant higher 3.3 ± 0.44 fold (p < 0.001) migration than the CFT073 strain. MG1655 was also shown to attract the largest number of PMN compared to the other strains (Figure 3B). There were no differences observed between ESBL-producing and susceptible strains in their ability to attract PMN after 3 h (data not shown).

Bottom Line:
The ability of ESBL strains to evoke ROS-production from PMN cells was significantly higher than that of the non-ESBL strains.The number of migrating PMN was significantly higher in response to ESBL strains compared to non-ESBL strains.Stimulation of A498 cells with ESBL strains elicited lower production of IL-6 and IL-8 compared to non-ESBL strains.

Background: Infections caused by extended spectrum beta-lactamases (ESBL)-producing bacteria have been emerging worldwide and the majority of ESBL-producing E. coli strains are isolated from patients with urinary tracts infections. The purpose of this study was to compare the host-response mechanisms in human polymorphonucleated leukocytes (PMN) and renal epithelial cells when stimulated by ESBL- or non-ESBL-producing uropathogenic E. coli (UPEC) isolates. The host-pathogen interaction of these ESBL-producing strains in the urinary tract is not well studied.

Results: The ability of ESBL strains to evoke ROS-production from PMN cells was significantly higher than that of the non-ESBL strains. The growth of ESBL strains was slightly suppressed in the presence of PMN compared to non-ESBL strains after 30 min and 2h, but the opposite was observed after 5 and 6h. The number of migrating PMN was significantly higher in response to ESBL strains compared to non-ESBL strains. Stimulation of A498 cells with ESBL strains elicited lower production of IL-6 and IL-8 compared to non-ESBL strains.

Conclusion: Significant differences in host-response mechanisms were identified when host cells were stimulated by ESBL- or non-ESBL producing strains. The obtained results on the early interactions of ESBL-producing strains with the host immune system may provide valuable information for management of these infections.